Abstract Background: Topical corticosteroids (TCS) are the mainstay of treatment in atopic dermatitis (AD) flares. The fears and worries concerning TCS are known as corticophobia. Corticophobia is common in patients with AD and can lead to suboptimal TCS application and treatment failure. Health literacy (HL) may influence corticophobia. TOPICOP© and HLS-EU-PT questionnaires have been developed to evaluate corticophobia and HL, respectively. Objective: Evaluate the relationship between corticophobia and the degree of HL in patients with AD. Methods: Prospective cross-sectional study with AD patients followed at a Dermatology Department, between September 2019 and February 2020. Patients, or their parents (if patients had ≤ 15 years), were invited to answer TOPICOP© questionnaire, HLS-EU-PT questionnaire, and a disease characterization and demographic questionnaire. Results: We included 61 patients (57.4% females, mean age 20 ± 13.8 years, mean disease duration of 12.5 ± 11.4 years). TOPICOP© mean score was 44.8 ± 20.0 (8.3 to 88.9) and HLS-EU-PT mean score was 30.5 ± 8.5 (1.1 to 47.9). TOPICOP© score was negatively correlated with HLS-EU-PT score (p = 0.002, r = -0.382, r2 = 0.146). There was no statistical difference between TOPICOP© score and disease characteristics (disease severity, family history of AD or personal history of other atopic diseases). Study limitations: Small and heterogenous cohort composed of patients and patients’ parents. Conclusions: The degree of corticophobia is similar to the values reported in other studies. HL had an inverse correlation with corticophobia. Lower HL was shown to be a predictor of higher corticophobia. The promotion of health literacy is essential for the correct use of TCS and good control of AD.

Abstract Annular elastolytic giant cell granuloma is an uncommon granulomatous cutaneous disease that usually affects sun-exposed skin. Non-scarring alopecia is a possible presentation. Although histopathology is mandatory for the diagnosis, dermoscopy may help to narrow down the clinical differential diagnosis. The authors report a case of annular elastolytic giant cell granuloma in the scalp of a female adult patient, showing multiple yellowish/orange follicular dots in a diffuse erythemato-whitish background in the dermoscopy.

Abstract Ashy dermatosis is a pigmentation dermatosis that belongs to the group of acquired macular hyperpigmentation disorders of uncertain etiology. Although the adulthood forms usually occur in higher Fitzpatrick skin types, pediatric cases are more common in lower phototypes. The authors report two cases of pre-pubertal ashy dermatosis and perform a brief review of literature to highlight the differences in epidemiology and course of the disease in children and adults. etiology types phototypes prepubertal pre pubertal adults

Resumo A dermatose cinzenta é uma doença da pigmentação que pertence ao grupo dos distúrbios de hiperpigmentação macular adquirida de etiologia incerta. Embora as formas do adulto ocorram habitualmente em fotótipos cutâneos de Fitzpatrick elevados, os casos pediátricos são mais comuns em fotótipos baixos. Os autores reportam dois casos de dermatose cinzenta em idade pediátrica e descrevem uma breve revisão da literatura para salientar as diferenças de epidemiologia e de curso da doença em crianças e adultos. incerta elevados baixos adultos

RESUMO A disrupção da barreira cutânea é um dos achados característicos da dermatite atópica (DA), que inclui alterações no envelope cor-nificado, lamela lipídica, tightjunctions e microbioma cutâneo. Estas alterações estão também presentes na pele não lesada de doentes com DA, o que sugere que os defeitos da barreira epidérmica possam ser a etapa inicial no desenvolvimento da DA e, eventualmente, de outras doenças atópicas (marcha atópica). A evidência atual indica que a fisiopatologia da DA envolve uma interação entre esta barreira cutânea disfuncional e uma resposta imunitária inata e adaptativa predominantemente do tipo 2, que contribuem para a disrupção da barreira epidérmica através da ação de citocinas do tipo 2. Neste contexto, as anomalias da barreira permitem uma maior penetração dos alergénios ambientais e alimentares, que aumentam a suscetibilidade à sua sensibilização. Durante o processo de sensibilização, a linfopoietina do estroma tímico (TSLP) polariza as células dendríticas da pele para uma resposta T-helper 2, desempenhando também um papel chave na sensibilização da alergia alimentar, asma e rinite alérgicas. Nesta revisão, os autores descrevem o conhecimento atual da fisiopatologia da barreira epidérmica, a sua alteração na DA e influência no de-senvolvimento de comorbilidades atópicas e o papel da terapêutica de reparação da barreira na prevenção da progressão da marcha atópica.

ABSTRACT Impaired skin barrier is one of the hallmarks of atopic dermatitis (AD), with abnormalities in the cornified envelope, lipid lamellae, tight junctions and cutaneous microbiome. These findings are also present in nonlesional skin of AD individuals, suggesting that epidermal barrier defects may be the initial step towards the development of AD and eventually other atopic diseases (atopic march). It is currently known that pathophysiology of AD involves an interplay between this dysfunctional skin barrier and a predominantly type 2 skewed innate and adaptive immune responses, which further disrupt the skin barrier through type 2 cytokines. In this setting, there is enhanced penetration of environmental and food allergens through a deficient barrier, leading to an increased susceptibility to sensitization. During the sensitization process, thymic stromal lymphopoietin (TSLP) polarizes skin dendritic cells to a T-helper 2 response, and TSLP seems to be a key cytokine in the sensitization of food allergy, allergic asthma and rhinitis. In this review, the authors describe the current knowledge of the pathophysiology of the epidermal barrier, its disruption in AD and how it may be involved in the development of atopic comorbidities and the role of barrier repair therapy on the prevention of the atopic march progression.